Nuclear factor-κB and apoptosis in patients with intracerebral hemorrhage

Abstract

Studies using rat models have indicated that neuronal apoptosis is involved in the pathogenesis of intracerebral hemorrhage (ICH); however, the mechanism by which apoptosis occurs is unclear. In the present study, we aimed to quantify the number of nuclear factor-κB (NF-κB)-positive cells and apoptotic cells in specimens of middle temporal gyrus taken from 46 human subjects with hypertensive ICH. We also investigated the roles that intercellular adhesion molecule-1 (ICAM-1) and interleukin (IL)-1β play in apoptosis following ICH. At about 24 hours after ICH, some neurons exhibited nuclear swelling and incomplete cellular structures were visible. The mean percentage of apoptotic cells was 39.28 ± 21.83% at 49–72 hours after ICH. NF-κB immunoreactivity varied with time after ICH: the number of immunostained neurons increased during the 2–6 hours after ICH, and reached a maximum at 7–48 hours. The number of IL-1β-immunostained neurons reached a maximum at 2–6 hours after ICH. The number of ICAM-1-immunostained neurons increased during the 48 hours after ICH and reached a maximum at 49–72 hours. These observations indicate that apoptosis has a major role in pathological cell death after ICH and that activation of NF-κB is positively related to the progress of apoptosis. Additionally, activation of ICAM-1 and IL-1β seem to be involved in apoptosis after ICH.